Production of serum amyloid A and C-reactive protein by HepG2 cells

Stimulated with combinations of cytokines or monocyte conditioned media: The effects of prednisolone

J. W. Smith, Thomas L McDonald

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48 Citations (Scopus)

Abstract

The hepatic production of the acute phase proteins in response to inflammatory cytokines, and the interaction of corticosteroids within this response, has been the subject of considerable recent research. In this study we have examined the effects of the corticosteroid prednisolone on the production of IL-1α and IL-1β by lipopolysaccharide (LPS)-stimulated monocytes, and the ability of the monocyte conditioned media (MOCM) obtained under these conditions to induce human hepatoma HepG2 cells to produce serum amyloid A (SAA) and C-reactive protein (CRP). We also examined the production of SAA and CRP by HepG2 cells exposed to different combinations and concentrations of recombinant human (rh) IL-1α, rhIL-1β, rhIL-6, recombinant human tumour necrosis factor-alpha (rhTNF-α) and prednisolone. The findings indicate: (i) prednisolone substantially inhibits the production of both IL-1α and IL-1β by LPS-stimulated monocytes. The MOCM from prednisolone-treated monocytes induced less SAA and CRP production by HepG2 cells; (ii) IL-1α and IL-1β both induced CRP and SAA synthesis by HepG2 cells, but only in the presence of IL-6. IL-1β was the more potent inducer for SAA production, but for CRP production IL-1α and IL-1β were equivalent; (iii) prednisolone enhances the production of SAA by HepG2 cells, but does not enhance the production of CRP; (iv) TNF-α in the presence or absence of IL-6 and/or prednisolone did not induce the production of SAA or CRP by HepG2 cells. These findings offer a tenable solution to a disparate production of SAA compared with CRP in corticosteroid-treated cystic fibrosis (CF) patients.

Original languageEnglish (US)
Pages (from-to)293-299
Number of pages7
JournalClinical and Experimental Immunology
Volume90
Issue number2
StatePublished - Jan 1 1992

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Serum Amyloid A Protein
Hep G2 Cells
Conditioned Culture Medium
Prednisolone
Interleukin-1
C-Reactive Protein
Monocytes
Cytokines
Adrenal Cortex Hormones
Lipopolysaccharides
Interleukin-6
Acute-Phase Proteins
Cystic Fibrosis
Hepatocellular Carcinoma
Tumor Necrosis Factor-alpha

Keywords

  • C-reactive protein
  • HepG2
  • corticosteroids
  • cytokines
  • serum amyloid A

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

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abstract = "The hepatic production of the acute phase proteins in response to inflammatory cytokines, and the interaction of corticosteroids within this response, has been the subject of considerable recent research. In this study we have examined the effects of the corticosteroid prednisolone on the production of IL-1α and IL-1β by lipopolysaccharide (LPS)-stimulated monocytes, and the ability of the monocyte conditioned media (MOCM) obtained under these conditions to induce human hepatoma HepG2 cells to produce serum amyloid A (SAA) and C-reactive protein (CRP). We also examined the production of SAA and CRP by HepG2 cells exposed to different combinations and concentrations of recombinant human (rh) IL-1α, rhIL-1β, rhIL-6, recombinant human tumour necrosis factor-alpha (rhTNF-α) and prednisolone. The findings indicate: (i) prednisolone substantially inhibits the production of both IL-1α and IL-1β by LPS-stimulated monocytes. The MOCM from prednisolone-treated monocytes induced less SAA and CRP production by HepG2 cells; (ii) IL-1α and IL-1β both induced CRP and SAA synthesis by HepG2 cells, but only in the presence of IL-6. IL-1β was the more potent inducer for SAA production, but for CRP production IL-1α and IL-1β were equivalent; (iii) prednisolone enhances the production of SAA by HepG2 cells, but does not enhance the production of CRP; (iv) TNF-α in the presence or absence of IL-6 and/or prednisolone did not induce the production of SAA or CRP by HepG2 cells. These findings offer a tenable solution to a disparate production of SAA compared with CRP in corticosteroid-treated cystic fibrosis (CF) patients.",
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N2 - The hepatic production of the acute phase proteins in response to inflammatory cytokines, and the interaction of corticosteroids within this response, has been the subject of considerable recent research. In this study we have examined the effects of the corticosteroid prednisolone on the production of IL-1α and IL-1β by lipopolysaccharide (LPS)-stimulated monocytes, and the ability of the monocyte conditioned media (MOCM) obtained under these conditions to induce human hepatoma HepG2 cells to produce serum amyloid A (SAA) and C-reactive protein (CRP). We also examined the production of SAA and CRP by HepG2 cells exposed to different combinations and concentrations of recombinant human (rh) IL-1α, rhIL-1β, rhIL-6, recombinant human tumour necrosis factor-alpha (rhTNF-α) and prednisolone. The findings indicate: (i) prednisolone substantially inhibits the production of both IL-1α and IL-1β by LPS-stimulated monocytes. The MOCM from prednisolone-treated monocytes induced less SAA and CRP production by HepG2 cells; (ii) IL-1α and IL-1β both induced CRP and SAA synthesis by HepG2 cells, but only in the presence of IL-6. IL-1β was the more potent inducer for SAA production, but for CRP production IL-1α and IL-1β were equivalent; (iii) prednisolone enhances the production of SAA by HepG2 cells, but does not enhance the production of CRP; (iv) TNF-α in the presence or absence of IL-6 and/or prednisolone did not induce the production of SAA or CRP by HepG2 cells. These findings offer a tenable solution to a disparate production of SAA compared with CRP in corticosteroid-treated cystic fibrosis (CF) patients.

AB - The hepatic production of the acute phase proteins in response to inflammatory cytokines, and the interaction of corticosteroids within this response, has been the subject of considerable recent research. In this study we have examined the effects of the corticosteroid prednisolone on the production of IL-1α and IL-1β by lipopolysaccharide (LPS)-stimulated monocytes, and the ability of the monocyte conditioned media (MOCM) obtained under these conditions to induce human hepatoma HepG2 cells to produce serum amyloid A (SAA) and C-reactive protein (CRP). We also examined the production of SAA and CRP by HepG2 cells exposed to different combinations and concentrations of recombinant human (rh) IL-1α, rhIL-1β, rhIL-6, recombinant human tumour necrosis factor-alpha (rhTNF-α) and prednisolone. The findings indicate: (i) prednisolone substantially inhibits the production of both IL-1α and IL-1β by LPS-stimulated monocytes. The MOCM from prednisolone-treated monocytes induced less SAA and CRP production by HepG2 cells; (ii) IL-1α and IL-1β both induced CRP and SAA synthesis by HepG2 cells, but only in the presence of IL-6. IL-1β was the more potent inducer for SAA production, but for CRP production IL-1α and IL-1β were equivalent; (iii) prednisolone enhances the production of SAA by HepG2 cells, but does not enhance the production of CRP; (iv) TNF-α in the presence or absence of IL-6 and/or prednisolone did not induce the production of SAA or CRP by HepG2 cells. These findings offer a tenable solution to a disparate production of SAA compared with CRP in corticosteroid-treated cystic fibrosis (CF) patients.

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